KEY POINTS: There is assumed to be a monotonic association between melatonin suppression and circadian phase resetting induced by light exposure. We tested the association between melatonin suppression and phase resetting in humans. Sixteen young healthy participants received nocturnal bright light ( approximately 9500 lux) exposure of continuous or intermittent patterns, and different durations ranging from 12 min to 6.5 h. Intermittent exposure patterns showed significant phase shifts with disproportionately less melatonin suppression. Each and every bright light stimulus in an intermittent exposure pattern induced a similar degree of melatonin suppression, but did not appear to cause an equal magnitude of phase shift. These results suggest that phase shifts and melatonin suppression are functionally independent such that one cannot be used as a proxy measure of the other. ABSTRACT: Continuous experimental light exposures show that, in general, the conditions that produce greater melatonin suppression also produce greater phase shift, leading to the assumption that one can be used as a proxy for the other. We tested this association in 16 healthy individuals who participated in a 9-day inpatient protocol by assessing melatonin suppression and phase resetting in response to a nocturnal light exposure (LE) of different patterns: (i) dim-light control (<3 lux; n = 6) or (ii) two 12-min intermittent bright light pulses (IBL) separated by 36 min of darkness ( approximately 9500 lux; n = 10). We compared these results with historical data from additional LE patterns: (i) dim-light control (<3 lux; n = 11); (ii) single continuous bright light exposure of 12 min (n = 9), 1.0 h (n = 10) or 6.5 h (n = 6); or (iii) an IBL light pattern consisting of six 15-min pulses with 1.0 h dim-light recovery intervals between them during a total of 6.5 h (n = 7). All light exposure groups had significantly greater phase-delay shifts than the dim-light control condition (P < 0.0001). While a monotonic association between melatonin suppression and circadian phase shift was observed, intermittent exposure patterns showed significant phase shifts with disproportionately less melatonin suppression. Each and every IBL stimulus induced a similar degree of melatonin suppression, but did not appear to cause an equal magnitude of phase shift. These results suggest unique specificities in how light-induced phase shifts and melatonin suppression are mediated such that one cannot be used as a proxy measure of the other.

The focus of sustainable lighting tends to be on reduced CO2 emissions and cost savings, but not on the wider environmental effects. Ironically, the introduction of energy-efficient lighting, such as light emitting diodes (LEDs), may be having a great impact on the health of wildlife. These white LEDs are generated with a high content of short-wavelength 'blue' light. While light of any kind can suppress melatonin and the physiological processes it regulates, these short wavelengths are potent suppressors of melatonin. Here, we manipulated the spectral composition of LED lights and tested their capacity to mitigate the physiological and health consequences associated with their use. We experimentally investigated the impact of white LEDs (peak wavelength 448 nm; mean irradiance 2.87 W/m(2) ), long-wavelength shifted amber LEDs (peak wavelength 605 nm; mean irradiance 2.00 W/m(2) ), and no lighting (irradiance from sky glow < 0.37 x 10(-3) W/m(2) ), on melatonin production, lipid peroxidation, and circulating antioxidant capacity in the tammar wallaby (Macropus eugenii). Night-time melatonin and oxidative status were determined at baseline and again following 10 weeks exposure to light treatments. White LED exposed wallabies had significantly suppressed nocturnal melatonin compared to no light and amber LED exposed wallabies, while there was no difference in lipid peroxidation. Antioxidant capacity declined from baseline to week 10 under all treatments. These results provide further evidence that short-wavelength light at night is a potent suppressor of nocturnal melatonin. Importantly, we also illustrate that shifting the spectral output to longer wavelengths could mitigate these negative physiological impacts.

Humans are lighting the night-time environment with ever increasing extent and intensity, resulting in a variety of negative ecological effects in individuals and populations. Effects of light at night on reproductive fitness traits are demonstrated across taxa however, the mechanisms underlying these effects are largely untested. One possible mechanism is that light at night may result in perturbed reactive oxygen species (ROS) and oxidative stress levels. Here, we reared Drosophila melanogaster under either dim (10 lx) light or no light (0 lx) at night for three generations and then compared mating and lifetime oviposition patterns. In a second experiment, we explored whether exposure to light at night treatments resulted in variation in ROS levels in the heads and ovaries of six, 23- and 36-day-old females. We demonstrate that dim light at night affects mating and reproductive output: 10 lx flies courted for longer prior to mating, and female oviposition patterns differed to 0 lx females. ROS levels were lower in the ovaries but not heads, of 10 lx compared with 0 lx females. We suggest that reduced ROS levels may reflect changes in ovarian physiology and cell signaling, which may be related to the differences observed in oviposition patterns. Taken together, our results indicate negative consequences for invertebrates under more stressful, urban, lit conditions and further investigation into the mechanisms driving these changes is warranted to manage invertebrate communities in a brighter future.

Artificial Light At Night (ALAN) has several adverse impacts on biodiversity, and it has been recently used as a proxy to monitor human encroachment on landscapes at large spatial scales. The extent to which ALAN affects protected areas (PAs) and biodiversity hotspots (BHs) remains however untested at large spatial scales. We used this proxy to assess the spatial and temporal trends in the anthropization at a global scale within and around PAs and BHs. We found that ALAN is low and stable over time within PAs, but is the highest in a first outer belt (<25 km) around PAs, and tends to increase in a second outer belt (25–75 km). In the meantime, ALAN is higher within BHs than outside, and is even the highest and increasing over time in an inner belt, close to their periphery. Our results suggest that although PAs are creating safety zones in terms of ALAN, they tend to be more and more isolated from each other by a concentric human encroachment. In contrast, BHs are submitted to an increasing human pressure, especially in their inner periphery. Overall, we suggest integrating ALAN in large-scale conservation policies.

OBJECTIVE: The exposure to artificial light at night (ALAN) disrupts the biological rhythms and has been associated with the development of metabolic syndrome. MicroRNAs (miRNAs) display a critical role in fine-tuning the circadian system and energy metabolism. In this study, we aimed to assess whether altered miRNAs expression in the liver underlies metabolic disorders caused by disrupted biological rhythms. RESULTS: We found that C3H/HePas mice exposed to ALAN developed obesity, and hepatic steatosis, which was paralleled by decreased expression of Rev-erbalpha and up-regulation of its lipogenic targets ACL and FAS in liver. Furthermore, the expression of Rev-erbalpha-targeting miRNAs, miR-140-5p, 185-5p, 326-5p and 328-5p were increased in this group. Consistently, overexpression of these miRNAs in primary hepatocytes reduced Rev-erbalpha expression at the mRNA and protein levels. Importantly, overexpression of Rev-erbalpha-targeting miRNAs increased mRNA levels of Acly and Fasn. CONCLUSION: Thus, altered miRNA profile is an important mechanism underlying the disruption of the peripheral clock caused by exposure to ALAN, which could lead to hepatic steatosis.

Obesity and Comorbidities Research Center, Institute of Biology, University of Campinas/UNICAMP, Campinas, SP, Brazil; Department of Structural and Functional Biology, Institute of Biology, University of Campinas/UNICAMP, Campinas, SP, Brazil